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PubMed1999

Retrograde amnesia: clinical and methodological caveats.

Several clinical and methodological caveats are outlined as they pertain to retrograde amnesia research, and data relevant to these caveats are presented. Three caveats in particular are noted in relation to recently published cases of marked retrograde amnesia; (i) temporal lobe epilepsy may influence memory for news events; (ii) there may be additional, unsuspected pathology in cases of amnesia, such as those with cerebral hypoxia; (iii) degree of media exposure is closely related to performance on the types of news events memory tests that are commonly used in retrograde amnesia research.

Adult↗
PubMed1999

P300 event-related potentials in probable dissociative generalized amnesia.

1. To investigate whether abnormalities in objective neurophysiologic measures are observable in patients with probable dissociative generalized amnesia, the P300 and N100 event-related potentials were evaluated in six such patients in both acute stage and after recovery from amnesia. Findings were compared with those in 12 age- and gender-matched healthy subjects. 2. While latencies did not differ from those of control subjects, P300 amplitudes in acute-stage recordings were lower than those in controls. Repeated recordings in the patients showed a significant increase in P300 amplitude after recovery from amnesia. 3. Amplitude and latency of N100 did not differ between the patient and control groups, nor changed significantly after retrieval of memory. 4. These findings suggest that some unknown biological and/or psychologic mechanisms that cause retrograde autobiographic amnesia may impair cognitive function as reflected in an objective neurophysiologic measure such as the P300.

Adolescent↗
PubMed2003

Transient global amnesia in a young adult with cyanotic heart disease.

The etiology of transient global amnesia is poorly understood, particularly in children and young adults. Transient global amnesia may follow a wide range of precipitating events. Proposed causes have included vascular event, seizure, and migraine. A young man with cyanotic congenital heart disease experienced an episode of transient global amnesia in the setting of polycythemia. Differential diagnosis of acute confusional episodes in children should include transient global amnesia, as well as confusional migraine, and should include evaluation for underlying coagulation abnormalities and polycythemia.

Adult↗
PubMed2003

Severe amnesia following a unilateral temporal lobe stroke.

A 60 year old right-handed man developed severe amnesia following a left medial temporal stroke as documented by cerebral MRI, MRA and SPECT scans. Neuropsychological evaluation 13 weeks after the stroke showed a profound retrograde amnesia characterised by memory loss for public facts and events over the previous four decades. In addition, autobiographical memory showed selective loss of personal episodic memory with relative preservation of personal semantic memory. The development of this degree of amnesia with these features following a unilateral temporal lobe lesion is unusual. The possible neuroanatomical mechanisms underlying the amnesia and how they relate to current theories of memory loss are discussed.

Amnesia↗
PubMed1984

Amnesia for criminal offences.

Nearly 10% of a sample of men charged with a variety of offences claimed amnesia for their offence. The amnesia occurred only among those who had committed violence and was most frequent following homicide. All the amnesics had a psychiatric disorder, four having a primary depressive illness and the remainder being almost equally divided between schizophrenia and alcohol abuse. None of the amnesias had any legal implications. The circumstances of the offences suggested a variety of mechanisms to account for the amnesia, including repression, dissociation and alcoholic black-outs. Psychological defence mechanisms were probably of some importance, even when alcohol was an important factor.

Adult↗
PubMed2003

Amnesia for traumatic events among recent survivors: a pilot study.

OBJECTIVE: Traumatic amnesia has been amply documented in the psychoanalytic literature but inconsistently in the research literature. METHOD: Six trauma were followed prospectively. Survivors were interviewed 7, 30, and 120 days following the traumatic event. Each interview documented in detail their recollections of the day of their trauma. RESULTS: In four subjects who did not develop posttraumatic stress disorder (PTSD), we found brief, stable, and persistent memory gaps, which coincided with the moment of greatest emotional intensity. In two subjects who developed PTSD, we found, in addition to the previous form of amnesia, longer, progressive, and unstable memory gaps. DISCUSSION: Neurobiological research offers two explanatory mechanisms for the observations: A failure of acquisition of episodic memories may account for the stable deficits seen in all subjects. This could coincide with stress-induced malfunction of the hippocampal declarative memory system. A failure of spontaneous recall may account for the more extended traumatic amnesia that was observed in PTSD patients. This resembles the psychoanalytic description of repression. CONCLUSION: These preliminary findings suggest that brief, irreversible memory gaps are common in trauma survivors, whereas longer, progressive, and potentially reversible amnesia occurs among survivors who develop PTSD.

Adaptation, Psychological↗
PubMed1991

Selective hypnotic amnesia: is it a successful attempt to forget or an unsuccessful attempt to remember?

Subjects in 2 experiments (ns = 72 and 50) learned a 16-item, 4-category word list and were then administered hypnotic suggestions to be amnesic for all the words in 1 of the categories. Even when selective amnesia was completely successful, subjects in both experiments revealed a high level of recall for words not targeted for amnesia; moreover, these words were recalled in a highly organized, category-by-category fashion. Evidently, attention to relevant retrieval (i.e., organizational) cues does not oblige recall of words targeted for amnesia. Forgetting in the presence of such powerful mnemonic cues seems to characterize hypnotic amnesia and some spontaneous forms of forgetting as well. We argue that mnemonic lapses of this kind represent a failed attempt to remember rather than a successful attempt to forget.

Amnesia↗
PubMed1989

Increasing contextual pressures to breach posthypnotic amnesia.

The study investigated conditions that produce strong social pressures on posthypnotically amnesic Ss to remember more before being given the cue to remove amnesia. Highly susceptible Ss who passed posthypnotic amnesia were classified as voluntary or involuntary (having high or low control over recall). Test Ss were serially subjected to 3 pressure situations before being given the cue to lift amnesia: (a) instructions to be honest, (b) lie detection, and (c) a replay of a video of the session. Control Ss sat for the same amount of time and were only asked if they could remember anything else while the experimental Ss received the pressure recalls. All but 1 S breached in the experimental condition. Only the voluntary Ss breached in the control condition. Results are discussed as they relate to breaching amnesia and the voluntary dimension.

Amnesia↗
PubMed1985

Priming across modalities and priming across category levels: extending the domain of preserved function in amnesia.

Amnesia is considered to reflect the effects of damage to a specific brain system required for elaboration, consolidation, and conscious recollection. The study of amnesia is therefore a useful approach for establishing dissociations of function and for understanding the normal organization of memory functions. Amnesic patients and two control groups were tested in two studies of priming. In the first experiment, as measured by a word completion test, all groups exhibited significant priming effects that were greater within a modality than across modalities. The amnesic patients exhibited normal priming effects both within and across modalities, despite severe impairment in recall. In the second experiment, all groups exhibited significant and equivalent priming of category exemplars when category labels were presented and subjects were asked to produce the first exemplars that came to mind. The results extend the domain in which preserved priming effects can be observed in amnesia and they suggest that features of priming observed in normal subjects describe a capacity that is independent of the brain system damaged in amnesia.

Adult↗
PubMed2003

Interidentity amnesia for neutral, episodic information in dissociative identity disorder.

Interidentity amnesia is considered a hallmark of dissociative identity disorder (DID) in clinical practice. In this study, objective methods of testing episodic memory transfer between identities were used. Tests of both recall (interference paradigm) and recognition were used. A sample of 31 DID patients was included. Additionally, 50 control subjects participated, half functioning as normal controls and the other half simulating interidentity amnesia. Twenty-one patients subjectively reported complete one-way amnesia for the learning episode. However, objectively, neither recall nor recognition scores of patients were different from those of normal controls. It is suggested that clinical models of amnesia in DID may be specified to exclude episodic memory impairments for emotionally neutral material.

Adult↗
PubMed1977

Effects of d-amphetamine and strychnine on cycloheximide- and diethyldithiocarbamate-induced amnesia in mice.

Groups of C57BL/6J mice were administred cycloheximide (CYC) 30 min before or immediately after training on a passive avoidance task and tested 72 hr later. Some CYC-pretreated groups were given strychnine or d-amphetamine (d-amp) immediately after training and others were given d-amp 1 hr after training. Other groups were given diethyldithiocarbamate (DDC) at various times before or after training. Some DDC-pretreated groups were gived-amp or strychnine as described above for CYC groups. Immediate posttraining administration of 5 mg/kg d-amp, but not strychnine, prevented amnesia in CYC-pretreated mice. The DDC induced an apparent amnesia when administered from 30 min before training to 3 hr after training. Posttraining administration of d-amp or strychnine did not prevent DDC-induced amnesia. These results are discussed in relation to previous suggestions that CYC- and DDC-induced amnesia may be the result of a functional impairment of catecholamine neurotransmitter systems by these drugs.

Amnesia↗
PubMed1989

Suggested posthypnotic amnesia in four diagnostic groups of hospitalized psychiatric patients.

We studied the parameters of suggested posthypnotic amnesia (initial deficit in recall, reversibility, and temporal disorganization of the initial material partially recalled during amnesia) in 132 psychiatric inpatients with DSM-III diagnoses of schizophrenia (N = 25), eating disorders (N = 77), alcoholism (N = 12), and major affective disorder (depression) (N = 18). We compared the findings on these patients with normal student control groups on the Stanford Hypnotic Susceptibility Scale (SHSS:C) posthypnotic suggestion item. In general, the small patient subgroups showed posthypnotic amnesia on each of these criteria in similar fashion to normal student populations. Highly hypnotizable patients were more likely to recall their hypnotic experiences in a more random order than the temporally more accurate sequence shown by low-hypnotizable subjects. Schizophrenic patients initially recalled fewer of their hypnotic experiences (indicating some cognitive deficit), and eating disorder patients initially recalled more of their experiences than other patient groups or normal subjects. Nevertheless, all patient subgroups showed significant additional recall after the reversibility cue. The results support the robustness of posthypnotic amnesia in psychiatric patients.

Adult↗
PubMed1996

Hypnotic amnesia and learning: a dissociation interpretation.

The effect of hypnotically induced amnesia on positive transfer learning was examined within the conceptual framework of dissociation theory. An Experimental group learned two paired-associates word lists that contained highly similar (between the two lists) stimulus words. After learning the first list, subjects were given suggestions for amnesia for that list. Control group 1 learned the same two lists without amnesia suggestions. Control group 2, with amnesia suggestions following the first list, learned two lists that contained dissimilar stimulus words. All subjects remained hypnotized throughout the session. Positive transfer between the two lists was demonstrated for the Experimental group and for Control group 1, but not for Control group 2. The results are viewed as consistent with predictions from dissociation theory.

Amnesia↗
PubMed1999

Posthypnotic amnesia for material learned before hypnosis.

The impact of a suggestion for posthypnotic amnesia on material learned either before or during hypnosis was investigated across 2 experiments. In Experiment 1, very high, high, and low hypnotizable participants learned a word list either before or immediately after a hypnotic induction. During hypnosis, participants were given a suggestion for posthypnotic amnesia for the word list. After hypnosis, they were tested on recall, word-fragment, and word-recognition tasks. Experiment 2 replicated and extended Experiment 1 through application of the real-simulating paradigm. Across the 2 experiments, there was no difference in the performance of participants who learned the word list either before or during hypnosis. Although amnesia on direct memory measures was associated with high hypnotizability (Experiment 1), an explanation based on demand characteristics could not be excluded (Experiment 2). The implications of these findings for the use of post-hypnotic amnesia as a laboratory analog of disorders of autobiographical memory are discussed.

Adult↗
PubMed2004

Is traumatic amnesia nothing but psychiatric folklore?

Some psychotherapists believe that certain experiences are so overwhelmingly traumatic that some victims become incapable of remembering their worst trauma except under special circumstances (e.g. therapy) many years later. Unfortunately, clinicians who endorse this concept of traumatic amnesia often misinterpret the very studies they adduce in support of it. More specifically, they misinterpret other, unrelated memory phenomena as evidence for traumatic amnesia, such as ordinary forgetfulness, psychogenic amnesia, organic amnesia, incomplete encoding of traumatic experiences, non-disclosure of remembered trauma, and simply not thinking about something for a long time. The purpose of this article is to dispel confusions rampant in this literature.

Amnesia↗
PubMedDate not supplied

How can be best explain retrograde amnesia in human memory disorder?

I firstly consider general issues relating to our attempts to understand retrograde amnesia. Three main hypotheses are reviewed that have been proposed to account for retrograde amnesia. A theory is outlined to explain the dense autobiographical amnesia that is a focal phenomenon in some cases of severe head injury. This theory postulates that autobiographical retrieval requires the activation of a distributed network of cognitive operations, and that autobiographical amnesia results from the occurrence of multiple areas of pathology, distributed over both space and time.

Age Factors↗
PubMed2001

Focal cerebral hyperemia in postconcussive amnesia.

Transient amnesia caused by minor head injury is commonly encountered in daily neurosurgical practice, but the mechanism of such amnesia has not been extensively studied. We measured the regional cerebral blood flow (rCBF) of patients with postconcussive amnesia with Xe/CT CBF to examine whether a focal disturbance of CBF exists. The Xe/CT CBF study was performed in eight patients with closed head injury without organic cerebral lesion while they were suffering from posttraumatic amnesia (concussion group). The time interval between accident and CBF measurement was less than 2 h in three patients, 5-6 h in two, 8-9 h in two, and 18 in one. The results were compared with those of nine normal volunteers and eight other age-matched patients who recovered without any neurological deficit despite the presence of hemorrhagic regions (mild hemorrhage group). The rCBF of the concussion group was significantly elevated in the bilateral mesial temporal cortex in comparison to the normal group. The rCBF in the mild hemorrhage group was lower than that of normal controls in all regions. The analysis of right-left difference in CBF indicated that there was significant asymmetry (right > left) in the frontal and temporal cortex in the concussion group, but not in the normal and mild hemorrhage group. This Xe/CT CBF study in acute stages of cerebral concussion, in which patients were amnestic, detected focal cerebral hyperemia. Such hyperemia in regions closely related to human memory function may be the result of vasoparalysis or the compensatory activation of memory circuits after denervation injury.

Adolescent↗
PubMed1985

A contribution to the anatomical basis of thalamic amnesia.

Damage to diencephalic structures is stated to give rise to memory dysfunction. Amnesia is likely to occur following vascular lesions in the ventral portion of the thalamus. The CT findings of 6 of our own cases and 5 patients reported in the literature, all with selective vascular lesions of the thalamus, were studied to determine the critical structures involved in human memory processes more closely. Thalamic amnesia probably depends on intrathalamic white matter lesions more than on nuclear lesions. The mamillothalamic tract and the ventral portion of the lamina medullaris interna are the most likely candidates in the mediation of memory processes and a combined lesion of these structures may be responsible for thalamic amnesia in man. Two patients without significant memory dysfunction had lesions in the ventrobasal portion of the mediodorsal nucleus sparing the mamillothalamic tract and the ventral part of the lamina medullaris interna. Our findings correspond well with the understanding of amnesia as a 'disconnection syndrome' stressed recently by Warrington and Weiskrantz (1982) and with Mishkin's (1982) model of the memory system in monkeys.

Aged↗